HY lecture notes:
Random point for pediatrics is that pregnancy can occur before one’s first period, so if they give you, e.g., a 13F who’s never had a menstrual period but who presents with signs and symptoms suggestive of pregnancy (i.e., nausea/vomiting, suprapubic mass, etc.), consider pregnancy as an answer. One of the pediatric forms has a Q where the answer was “beta-hCG” in this scenario.
HY is differentiating polycystic ovarian syndrome (PCOS) from hypothyroidism from Cushing syndrome. This applies to pediatrics as well and there are many questions on it.
High BMI female + irregular menstrual cycles –> anovulation.
Anovulation + hirsutism –> PCOS.
Anovulation. Cause USMLE wants? –> insulin resistance –> causes abnormal GnRH pulsation.
Why hirsutism in anovulation –> abnormal GnRH pulsation causes high LH/FSH ratio.
Why high LH/FSH ratio important in anovulation/PCOS –> ovulation stimulated when follicle not ready –> no ovulation (anovulation) –> follicle retained as cyst.
What’s LH do? –> Stimulates theca interna cells (females) and Leydig cells (males) to make androgens.
What’s FSH do? –> Stimulates granulosa cells (females) and Sertoli cells (males) to make aromatase; also primes follicles.
Tx for PCOS –> if high BMI, weight loss first always on USMLE.
Tx for PCOS if they ask for meds and/or weight loss already tried –> OCPs (if not wanting pregnancy); clomiphene (if wanting pregnancy).
PCOS increases risk of what –> endometrial cancer (unopposed estrogen).
PCOS will present on the USMLEs + various shelf exams as missed periods, not gradually prolonged periods. The cysts are the result of follicles that literally did not rupture, meaning ovulation does not occur.
14F + low mood + gradually increasing fatigue + menstrual cycles gradually increasing in length + BMI 26; Dx? –> hypothyroidism (Hashimoto).
16F + proximal muscle weakness + increased creatine kinase + low mood + fatigue; Dx? –> Hashimoto.
15MM + decreased ability to get up from chair unassisted + HR 60; Dx? –> Hashimoto.
17M + total cholesterol 300 mg/dL + high hepatic AST + HR 55; Dx? –> Hashimoto (hypothyroidism can cause bradycardia, high cholesterol, and high AST [the latter is weird, correct]).
Hashimoto parameters –> high TSH, low T3, low T4, decreased iodine uptake
Mechanism for Hashimoto –> antibodies against thyroperoxidase + thyroglobulin; anti-microsomal.
Histo of Hashimoto –> lymphocytic infiltrate (asked on one of the 2CK NBME forms weirdly enough).
Tx for Hashimoto = levothyroxine (synthetic T4).
Key point regarding menstruations is that periods gradually increase in length + become heavier; although hypothyroidism and PCOS can present with amenorrhea, PCOS won’t present with gradually increasing length + heaviness the same way hypothyroidism will.
Cushing disease Qs can present with either increased length of menstrual cycle + heaviness of periods, or missed periods altogether (insulin resistance –> anovulation/PCOS). However you’ll be able to differentiate in the vignette because they’ll throw in other signs of Cushing like purple striae.
One Cushing Q on a 2CK form gave just gradually increasing heaviness of periods + acanthosis nigricans –> the reason the answer wasn’t PCOS is because, once again, we’d expect missed periods with PCOS.
It is suspected that the mechanism for menstrual dysfunction in hypothyroidism is as follows: low T3/T4 –> decreased negative feedback at hypothalamus –> increased TRH –> increased prolactin release –> GnRH dysfunction. It should be noted that prolactin is regulated two ways: 1) dopamine inhibits prolactin release, and 2) TRH (not TSH) directly stimulates it.
Should also be noted that Cushing disease in children can present as precocious puberty and/or stunted growth, rather than as Cushingoid appearance.
